Serum from diabetic patients, as well as having high levels of glucose
and ketone bodies, is known to have embryotoxic and teratogenic effec
ts that play an important role in diabetes-induced teratology. We stud
ied the effect of serum from women with gestational diabetes, who are
not known to have a high incidence of malformations in their offspring
, on the in vitro development of 10.5-day-old rat embryos. Results fro
m these studies were then compared with those using serum from pregnan
t women with Type I diabetes, serum from pregnant women without diabet
es, and normal rat serum. Serum from pregnant women with Type I diabet
es caused abnormalities in 71% of the embryos in comparison with an in
cidence of 53.3% in embryos cultured in serum from women with gestatio
nal diabetes. Embryos cultured in serum from women without diabetes or
in rat serum had a 9 and 4.2% incidence of defects, respectively. Dia
betic serum also decreased the size of the embryos, the number of somi
tes, yolk sac diameter, and the amount of protein in the embryos and t
heir yolk sacs. This damage was more significant when embryos were cul
tured in Type I diabetic serum than in serum from patients with gestat
ional diabetes. The levels of serum glucose, glycosylated haemoglobin,
fructosamine, beta-hydroxybutyrate (beta-HOB) and acetoacetate were a
lso higher in Type I diabetic serum than in serum from gestational dia
betes. Significant ultrastructural damage was observed in the yolk sac
s of embryos cultured in diabetic serum, with a reduction in the endoc
ytic index. The fact that serum from women with gestational diabetes i
s teratogenic to early somite rat embryos supports the hypothesis that
metabolic factors are responsible for diabetes-induced teratogenicity
and that to prevent these defects it is essential to stabilize the di
abetic state of the mother before, and during, early gestation.